Often times , there is a significant histo-pathological overlap between severe degrees of Ischemia* and myocyte necrosis . (What is called micro infarcts, lacunar infarcts, make us over diagnose MI). It is not yet clear , whether leaky myocyte cell membrane can release free cytoplasmic enzymes without actual cell necrosis.

Clinical Implication

Fortunately , there is not much .These bio markers are primarily used as prognostication tools .Many of these patients need to undergo early revascularisation. However , It is unwise,to get alarmed by just Troponin positivity in an other wise comfortable ACS patient.

* Some call severe degrees of Ischemia as Injury ! It is an old thought based entirely on ECG .There is no specific cellular equivalent of electrical injury current !

This is a true story . . . happened many years ago under my direct vision.

A 48 year old women came with significant breathlessness and catchy sub -sternal chest pain .

“I was exerting too much in recent days doctor” , she said .

Her ECG showed a tachycardia and dramatic ST depression in most leads .

The ER in charge promptly texted the cardiologist .

The moment he saw the ECG ,he had no hesitation , to order for an emergency angioplasty ( How can he plan a angioplasty , without even knowing the coroanry anatomy . some one murmured . May be . . what he probably meant was emergency angiogram the other explained ) Further , he was telling his fellows . . . that this is going top be tough case and a possible left main PCI .

An emergency angiogram was done . On table it was a huge surprise for every one , it was a a classical text book look alike normal coronary arteries !

The moment normal CAG was visualized the consultant concealed his momentary surprise and went on to say it is classical case of syndrome X with severe micro- vascular disease causing ECG changes !

As the patient did not give any opportunity to poke her coronaries she was wheeled out of wheeled out of cath lab.

Meanwhile , first year fellow came rushing with the blood reports and biochemistry .

He went on to say , don’t worry many times medicine is learnt in hard ways . After all nothing adverse has happened here .

The women was subsequently investigated and handed over to gynecologist for a probable hysterectomy .

Final message

Please be reminded , anemia can produce variety of ECG changes. In extreme anemia global ST depression is common especially if tachycardia is associated .

The lesson here is , whenever gross ST depression is witnessed with vague chest pain check the hemoglobin first . This is an unusual story of a women , with simple anemia (due to chronic mennorhagia ) landed in cath table in an acute fashion . Luckily she did not have any incidental coronary lesions that prevented her becoming a greater cath lab victim !

* The bewildered consultant is none other than the author of this blog.

This is the ECG of a 45 year old man with H/O hypertension and chest pain .The general practitioner who first saw him alerted this patient about a possible heart attack asked to meet a cardiologist immediately. The cardiologist who saw this ECG tended to confirm the diagnosis and advised admission in a coronary care unit .

The patient defied both and somehow landed in my echo lab . Looking at the ECG I also expected it to be a STEMI evolving into a Non Q MI .

I was surprised to find only LVH with absolutely no wall motion defect . There was no evidence of ASH, HOCM or apical cardiomyoapthy as one of my fellows initially suspected . His EF was 70 %. Cardiac enzymes were sent by then. When I spent few minutes with him , listening the history , it was very clear what he had was non cardiac pain . In the anxiety , no one got it right about the character of pain ,which was localised , lasted for few seconds and least suggesed angina.

The moral of the story is listen to the patient however dramatic the ECG may look !

What is special in this ECG ?

It is common for LVH with ST depression to be mistaken for ACS/NSTEMI

Here , there were other observations that added more complexity .

Presence of ST/T changes in inferior leads(ST elevation in lead 3)

Bi-phasic T wave in v1 to v3

ST elevation in precardial leads

In LVH it is usual to note ST depresion , how do you explain ST elevation in LVH ?

ST elevation in LVH may occur in leads v1 to v3 . It is very rare for LVH to inscribe ST elevation in v4 v5 v6 . Why certain leads elevate the ST segment while others depress in LVH is not clear. It may represent incomplete LBBB pattern where the ST segment deviates opposite to the dominant QRS complex. Septal hypertrophy often elevate while free wall hypertrophy depress the ST segment . Since V5,V6 leads are free wall oriented , these leads record classical ST depression .

Importance of Bi-Phasic T waves

Please remember Bi phasic T waves are notorious for it’s unpredictability. An innocuous looking bi-phasic T waves (especially with dynamic behavior ) is a harbinger of proximal LAD or even left main disease.

Finally , what will be ECG changes if a patient with classical LVH who develops a real STEMI ?

Acute STEMI is the numero uno of all medical emergencies. Hundreds of life are lost every few hours in our planet.Significant chunk of them do not even reach the hospital alive . While the emergency crew has many vital responsibilities , the cardiologist job starts only after the patient reaches the hospital . Hence the ambulance crew need to act much more sharper. Please remember even the skills of the driver will have a direct impact on the myocyte survival.

The symptom to first medical ( or second hospital ) contact could be as vital as a primary PCI procedure itself . A 3 minute traffic jam can kill 3 thousand myocytes ! One could imagine the importance of decision making process here.

Distance from the point of contact to PCI lab , the anticipated delay , intensity of traffic matters .

Is it not funny , to realise when we have a reperfusing agent on hand , within the ambulance and the vehicle stuck in the traffic jam waiting to reach a reperfusion room situated 50 km down the high way !

( One may wonder why can’t we thrombolyse every one routinely in the ambulance and do the PCI later in . . . But surprisingly this concept simply does not work !)

When we realise , even in a well developed country like Netherlands , time to shift to cath lab is a big issue (Read the following article ) we will never ever know , how much of myocardium is consumed by traffic jams in a country like India , where the traffic scenarios can be more chaotic than a VF !

Events that unfold following a STEMI are crucial

It begins with chest pain recognition.

Call for first help Spouse/Family doctor /Neighbor

Call for 911/108 . Ambulance arrival time and boarding

Administration of Aspirin + clopidogrel*

Meanwhile spontaneous thrombolysis will begin in most of them !

A promptly administered Aspirin and clopidogrel a shot of heparin and a lytic agent within 30 minutes is distinctly possible and may be more effective at a fraction of cost.

Highway thrombolysis

Even though current studies still . . .do not favor primary PCI over thrombolyiss in the first hour , most of the cardiologist do show some favoritism towards pPCI for some unknown reasons.

So by default , many of the ill fated STEMI patients enter an unrealistic hemodynamic race in the deadly highways and urban lanes our country !

For every minute that goes by , the patient not only loses his muscle but also the golden opportunity to get salvaged by the thrombolytic agents .

Since , a delay beyond one hour eliminates the indication of thrombolysis (if a cath lab is available in the vicinity ) many times traffic delays convert a potential hyperacute thrombolysis into a say . . . 3-6 hour old PCI .(Should we feel happy about it ?)

Helicopter drop over cath lab -( Distant dream ? or better to be in dreams ) It has been noticed even a helicopter was squarely beaten by the thrombolysis in terms of early and timely reperfusion.

Fast -Slow track PCI ? (Like fast slow AVNRT !)

Unexpected delays on road , in many countries financial issues /Insurance sanction etc contribute to the time delay significantly . What starts as a fast track protocol peters out into slow race (Late primary PCI ) and may even end in a grinding halt.(No primary PCI )

Worse still . . . some of these patients are made unsuitable for thrombolysis as well !

Final message

Management of STEMI is gradually becoming a team effort. The emergency crew , the command , the destination hospital all need to be alert and proactive. When the initial anticipated delay is getting prolonged , get the ground staff in cath lab ready for an emergency landing .

A word of advice for the ambulance crew .Involve them more in the decision making as they are in a better position to calculate the possible delay. If delays are anticipated propose a thrombolytic order and get clearance from the command and administer the lytic agent as early as possible.

It is highly likely , restoration of TIMI 2 flow right in the middle of national highways is much . . . better than a TIMI 3 flow that is going to come later . . .in a distant cath lab .

Finally use the common sense liberally before you act . . . unfortunately it has become the most elusive sense for man kind !

References :

Here is a study that gives a fresh insight into this enigmatic issue of pre-hospital thrombolysis vs primary PCI

By default most of us think , if it is NSTEMI . . . there must be ST depression. This thinking is not logical but traditional. Still, ST depression may be the common presentation. NSTEMI with ST depression has much worse outcome than other forms.

The following ECG is from a 45 year old man with a vague mid sternal chest pain for 48 hours.

There is a 2mm ST elevation , with a infarct as well ? But , the point here is there is no business for T waves to get bi-phasic or inverted in the early hours of a classical STEMI .

This exactly has happened here. Hence we can not call the above event as STEMI . Instead it is , STEMI evolving into NSTEMI . So a combination of features of STEMI/NSTEMI occur together. The best description for above entity is STEMI in transition to Non Q MI

No one exactly knows .It can be highly variable . So , 5 could be the correct answer .

* Most importantly hyper acute phase need not occur in all patients with STEMI as suggested in experimental models.

Some observations in T wave behavior in STEMI

Mechanism of hyper acute T waves

It is the pottsium channel dynamics.Transient intracellular hyperkalemia is thought to be responsible.

T wave as marker of reperfusion

Inverted T wave in precordial leads are a good marker of IRA patency especially in LAD

Slowly evolving STEMI

This is relatively new concept . STEMI with a prolonged hyper acute phase , ie , T waves ” dilly dallying” for hours or even few days have been recognised. (This was refered to pre-infarction angina in the past )

This sort of T wave behavior makes it difficult to diagnose STEMI.Enzymes will help , still thrombolytic guidelines demand us to wait till ST elevation to occur. This is unfortunate .But as physicians we are justified to thrombolyse tall T waves with a clinical ACS .The other simple solution is to shift the patient to cath lab to find what exactly is happening in the LAD !

Now , what is new about T waves in STEMI ?

It is the localizing value in LAD infarct

A tall persistent hyper acute T wave helps us to localise a LAD lesion .This paper from Netherlands , clearly confirms this observation. The study was done from a primary PCI cohort, a perfect setting to assess the T wave behavior in the early minutes /hours of STEMI .

Other mysteries about T waves in STEMI

Does hyperacute T waves occur in infero-posterior STEMI ?

I would believe it is very rare .Our CCU has not seen any tall T waves in inferior lead. Further analysis of the data from the above study could answer this question .

How often a hyperacute T waves transform into NSTEMI ?

This again is not clear.Most of the hyper acute T will evolve as STEMI .But , nothing prevents it to evolve as NSTEMI a well . After all , a hyper acute T MI can spontaneously lyse in a lucky few , ( Who has that critical mass of natural circulating TPA ) .If these natural lytic forces are only partially successful , it may evolve into de nova NSTEMI.

Bi-phasic T waves in ACS.

A benign looking T waves with terminal negativity in precordial leads can some times be a deadly marker of critical LAD disease.This has been notorious to cause deaths in young men which often correlates with the widow maker lesion in LAD.

The most bizarre aspect in our understanding about ACS pathophysiology is the concept of time window , based on which , all our ACS therapeutics revolve !

Does all myocardial cells have a same ischemic shelf life ? Can some patients be blessed with resistant myocardial cells when confronted with hypoxia or ischemia ?

It is well-known , in some hearts , the muscles go for necrosis within 30 minutes of ischemia, while some hearts can not be infarcted even after 24 hours of occlusion .So , slowly evolving STEMI is a feature of myocardial ischemic resistance .This is not a new phenomenon as we have extensively studied about the concept ischemic preconditioning .

We wonder there is something more to it . . . the quantum of preconditioning can be inherited .Further , we are grossly ignorant about the molecular secrets of non ischemic metabolic preconditioning .

Final message

T waves attract less attention in STEMI . Cardiologists are often tuned to look only the ST segment , after all , ACS itself is classified based on the behavior of this segment.(STEMI/NSTEMI) . We need to recognise ,there is a significant subset of ACS affecting exclusively T waves. Shall we call T elevation MI ? ( TEMI )

Do not ignore T waves in STEMI. It has more hidden electrophysiological treasures that is waiting to be explored .

Cleveland clinic is a leading centre for cardiac care .Major technological breakthrough occurs from this institute than any other place. Thousands of articles come out every year. Some articles , get global attention and make a huge impact. These are usually related to a new hi- tech modality like CRT devices or percutaneous aortic valve deployment etc ,etc.

Some articles , which are very important may not get the due attention . Journal editorial boards often have a scorecard called impact factor .That is , how a journal is impacting the practice habits of medical professionals . Ideally we need to have to grade individual articles with impact factor .Many articles may not have any significant impact however good the impact factor of the journal.

Here is an article, which excellently depicts the principles of management of ACS. It was published in 2003 JACC, by Steven Nissen from Cleveland, Ohio .It deserves more attention . Every cardiologist , involved in ACS management should read this, especially the interventionist.